Type I or Insulin-Dependent Diabetes Mellitus (IDDM) arises in genetically predisposed individuals as a consequence of immune-mediated destruction of the pancreatic islet insulin secreting cells. The onset of clinical symptoms of diabetes represents the end point of a chronic progressive decline in beta-cell function, and it appears only when the majority of beta-cells have been lost. Since IDDM develops insidiously, often years after the induction of the pathogenic immune-mediated destructive process, it can be predicted using immunological markers and tests of insulin secretion. The "Diabetes Prevention Trial of Type I Diabetes" (DPT-1) has been designed to test whether intervention during the prodromal period of the disease can delay its clinical onset. It is possible to identify impending clinical IDDM through the detection of autoantibodies against self-antigens of the pancreatic beta-cells. Since first degree relatives of probands with IDDM have more than ten-fold the risk of IDDM in the general population, the DPT-1 will focus on such relatives. Their initial blood (serum) screening will be for islet cell autoantibodies (ICA) detectable by the indirect immunofluorescence of cytoplasmic islet cell antigens in sections of normal human pancreas. Those individuals found to have ICA will then be staged into one of four different categories of risk of IDDM, dependent upon their point of progression to the clinical disease. IDDM risk assessment in non-diabetic relatives is based on a number of factors, including: genetic susceptibility, age, the presence of ICA especially if found together with insulin autoantibodies (IAA), and the degree of loss of first phase (1+3 minute) plasma insulin response (FPIR) during an intravenous glucose tolerance test (IVGTT). In the DPT-1, "High Risk" relatives will be those that have been predicted to have at least a 50 percent probability of developing IDDM within the next five years on the basis of positive ICA and low FPIR to IVGTT. Moderate risk relatives are those with positive ICA, but normal FPIR to IVGTT. This group is further divisible into those with an "Intermediate Risk' on account of positive IAA and those with only a 'Modest Risk' who are IAA negative. The 'Low Risk' relatives lack ICA. The purpose of dividing subjects into these four predictive risk groups is that different intervention strategies are best applied to them because of their stage of natural history, while the invasiveness of the therapeutic approaches to be tested needs to be appropriately reconciled with the estimated risk of IDDM in the different risk groups. In the "High Risk" group, the protocol is designed to determine whether parenteral insulin therapy, consisting of periodic courses of continuous intravenous insulin, with accompanying chronic subcutaneous insulin, will delay their expected development of clinical IDDM. The trial is a randomized, controlled, multicenter clinical trial, in which subjects randomized to an Experimental Group which will have the active intervention, while subjects randomized to the Standard Group will be closely monitored and offered treatment at the earliest sign of clinical IDDM. DPT-1 investigators acknowledge that a placebo-controlled, double-masked, multicenter clinical trial would be most desirable scientifically. Yet, the practicality of administering chronic subcutaneous placebo injections of a cloudy suspension and of admitting subjects for four days of periodic courses of continuous intravenous placebo infusions create numerous burdens for research subjects and place them at increased risk. This has led the investigators to select for the Standard Group a protocol is randomized, unmasked and without use of placebo, but one that involves close monitoring. The investigators recognize that this is a compromise, but appreciate it is in the best interest of those research subjects committing to this research alliance. Moreover, close observation and potential early intervention offers subjects randomized to the Standard Group the benefit of early diagnosis and the potential of early intervention for treatment of clinical IDDM. This is more than the standard of care in the general medical community for non-diabetic relatives. The intervention protocol for the "Intermediate Risk" group is designed to determine whether presentation of an islet cell autoantigen (i.e., orally-ingested insulin) to the immune system via the intestinal mucosa could induce disease-relevant immunological tolerance, thereby delaying the development of IDDM. This latter trial is designed to be a randomized, placebo controlled, double-masked, multicenter clinical trial, which will be staggered by six to twelve months after the initiation of randomization for the parenteral insulin trial. These two studies are envisioned to be the first in a series of studies designed to test the potential to prevent or delay the development of IDDM.